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. 2021 Jan 11;18(2):461–471. doi: 10.1038/s41423-020-00601-8

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — A model describing the mechanism regarding the inhibitory effect of taurocholic acid on the response to interferon-α therapy in patients with chronic hepatitis B. Compared with chronic hepatitis B (CHB) patients with low taurocholic acid (TCA) levels, CHB patients with high TCA levels had a lower number of CD3⁺CD8⁺ T and NK cells and lower levels of IFN-γ, TNF-α, granzyme B, and perforin secreted by CD3⁺CD8⁺ T and NK cells, resulting in the poor therapeutic response to pegylated interferon-alpha (PegIFNα) in CHB patients